IRON DEFICIENCY ANEMIA AND COMPENSATORY SNS ACTIVITY

缺铁和贫血的人类和大鼠无法维持身体 冷胁迫时的温度。 目前尚不清楚， 数据显示，这种体温调节缺陷在多大程度上是继发于 缺铁性贫血。 交换 输血可迅速改善体温维持， (TSH)反应、甲状腺素（T4）反应和三碘甲状腺原氨酸（T3） 缺铁动物对冷应激的反应。 升高 血浆和尿去甲肾上腺素（NE）水平不受 这种贫血的纠正。 代谢率的准确数据， 组织NE周转、甲状腺激素代谢或实际 缺乏与贫血相关的产热活性。 的 该提案的主要目标是确定 儿茶酚胺代谢降低体温调节 缺铁性贫血的症状 主要的假设是 测试的是，铁缺乏时SNS活性增加， 代偿性甲状腺激素功能可能受损 （改编自Cannon）。 有几个关键概念需要 作为潜在影响之前的中间目标 对缺铁性贫血的产热作用进行了研究。 第一个： 最低代谢和最大NE刺激 ID和对照组大鼠的代谢率不同， 贫血吗 第二：什么是静息代谢率关系 与对照组相比，ID中的温度？ 第三：是 交感神经系统活动增加ID在低 温度？ 贫血的潜在过程 铁缺乏可能影响产热， 定量血流量（微球）至产热 器官，甲状腺素转化为三碘甲状腺原氨酸的速率（肝脏 和棕色脂肪组织（5I-脱碘酶），BAT产热 活动（NE周转和线粒体。 GDP绑定）。 准确 记录IDA中代谢率和SNS活性将 为了解体温调节提供了良好的基础 缺陷 未来的研究可能会检查 组织铁缺乏对激素转换，受体部位 调节、线粒体功能障碍和/或CNS异常 控制产热。

Iron deficient and anemic humans and rats fail to maintain body temperature when cold stressed. It is not clear from existing data how much of this thermoregulatory defect is secondary to the anemic associated with iron deficiency. Exchange transfusion acutely improves body temperature maintenance, (TSH) response, thyroxine (T4) response and triiodothyronine (T3) response of iron deficient animals to a cold stress. Elevated plasma and urine norepinephrine (NE) levels are unaffected by this correction of anemia. Accurate data on metabolic rate, tissue NE turnover, thyroid hormone metabolism or actual thermogenic activity relative to the anemia are lacking. The major goal of this proposal is to define the relationships of catecholamine metabolism to decreased thermoregulatory capacity in iron deficiency anemia. The major hypothesis being tested is that increased SNS activity in iron deficiency is compensatory to perhaps impaired thyroid hormone function (model adapted from Cannon). Several key concepts need to be established as intermediate goals before the underlying effects of iron deficiency anemia on thermogenesis are examined. First: Are the minimum metabolic, and the maximal NE stimulated metabolic rates different in ID and control rats and affected by anemia? Second: What is the resting metabolic rate relationship to temperature in ID compared to controls? Third: Is sympathetic nervous system activity increased in ID at low temperatures? The underlying processes whereby the anemia of iron deficiency may affect thermogenesis are examined by quantification of blood flow (microspheres) to thermogenic organs, rates of conversion of thyroxine to triiodothyronine (liver and brown adipose tissue (5I-deiodinase), BAT thermogenic activity (NE turnover and mito. GDP binding). The accurate documentation of metabolic rate and SNS activity in IDA will provide a good base for understanding the thermoregulatory defects. Future studies may then examine possible effects of tissue iron deficiency on hormone conversion, receptor site regulation, mitochondrial dysfunction, and/or abnormal CNS control of thermogenesis.